Nasal Polyps: Epidemiology,
Pathology, Immunology, and
Treatment
Guy A. Settipane, M.D.
ABSTRACT
Nasal polyps frequently are associated with aspirin intoler-
ance, intrinsic asthma, Young's syndrome, cysticjibrosis, and
Kartagener's syndrome. Children 16 years or younger with
nasal polyps should be evaluated for cystic jibrosis. Nasal
polyps are frequently bilateral, multiple, freely movable, and
pale-gray and arise from the middle meatus of the nose.
Histologically, they classically have pseudostratijied ciliated
columnar epithelium, thickening of the epithelial basement
membrane, high stromal eosinophil count, mucin with neutral
pH, jew glands, and essentially no nerve endings. Cells consist
of a mixture q{ lymphocytes, plasma cells, and eosinophils.
Polyps from patients with Young's syndrome, Kartagener's
syndrome, and cystic jibrosis have predominately neutrophils
with insignijicant eosinophils. Chemical mediators found in
nasal polyps are as follows: histamine, serotonin, leukotrienes
[(SRS-A or LTC, LTD., LTE.), LTB.}. ECF-A, norepineph-
rine, kinins, TAME-esterase, and possibly PGD2. There is
more histamine in nasal polyps than in normal nasal mucosa,
and norepinephrine is present in greater concentration in the
base of nasal polyps than in normal mucosa. The concentra-
tions of IgA and IgE and, in some cases, IgG and IgM are
greater in polyp fluid than in serum. IgE-mediated disease is
not the cause of nasal polyps, but when present, may contribute
to episodes of exacerbation. Despite medical or surgical man-
agement, a significant number of nasal polyps are recurrent.
ror treatment, systemic corticosteroids should be tried before
surgical polypectomy. Polypectomy does not increase the risk
of developing asthma or making asthma worse. At the present
time, the pathogenesis of polyp formation is unknown.
Clinical Associate Professor, Brown University School of Med-
icine, and Director, Division of Allergy, Department ofMedi-
cine, Rhode Island Hospital, Providence
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INTRODUCTION
N asal polyps are frequently a manifestation of other
systemic disease. They may be associated with
asthma, aspirin intolerance (bronchospasm/urticaria),
cystic fibrosis, Kartagener's syndrome (chronic dyski-
netic cilia syndrome), and Young's syndrome (sinopul-
monary disease and azoospermia). In this review, the
following aspects of nasal polyps will be discussed:
historical background, epidemiology, anatomical pa-
thology, histopathology, differential diagnosis, chemical
mediators, pathogenesis, relationship to other diseases,
and types of treatment.
HISTORICAL BACKGROUND
T he existence of nasal polyps historically dates as far
back as 1000 B.C. Vancill has presented an excel-
lent historical survey of treatment for nasal polyps. In
about 400 B.c., Hippocrates developed two surgical
methods for nasal polypectomy: extraction by pulling
a sponge through the nasal canal and by cauterization.
Cato the Censor (234-149 B.c.) developed the first
known medical management of nasal polyps, using the
local application of herbs. Other ancient authors who
have written about nasal polyps through the centuries
are as follows: Celsus (42 B.C.-37 A.D.), Paulus of
Aegina (625-690 A.D.), Avicenna (980-1037 A.D.),
Saliceto (1210-1270 A.D.), Fallopius (1523-1562
A.D.), Petros Forestus (1522-1597 A.D.), Fabricius ab
Acquapendente (1537-1619 A.D.), Aranzi (1530-1589
A.D.), and Juncker, who in In I wrote: "According as
the moon fills or wanes, the polypi of the nose increase
or decrease in size. , ,," an excellent clinical observation
of remissions and exacerbations of polyps but certainly
a faulty lunar correlation. Thus, it appears that nasal
polyps have been a worrisome medical problem as far
back as man can remember.
119
EPIDEMIOLOGY tremely law, abaut 0.1 %.2,6 Any child 16 years ar
yaunger with nasal palyps shauld be evaluated far cystic
N asal palyps are still a challenge to. the physician
bath in diagnasis and treatment. They are mast fibrasis.
cam manly faund in nanatapic asthmatic patients aver
40 years af age, especially in thase patients with severe, ANATOMY

steraid-dependent asthma. The averall frequency af
nasal palyps in asthmatics between the ages af IOta
aver 50 years is 7% (Tables I and 11).2In a subgraup af
asthmatics, aver 40 years af age ar thase with negative
skin tests, the frequency ranges from 10-15% (Table
III).2 In patients with aspirin intalerance, the frequency
afnasal palyps may be as high as 36%.3,4Slavin'sgraup5
reparted an 33 patients with severe asthma and sinusi-
tis. Fifteen af these patients were receiving carticaste-
raids: 10 who. received cantinuaus carticasteraids and
5 who required intermittent bursts, Of these 33 patients,
30 ar 90% had a diagnasis af nasal palyps and 17 ar
52% had aspirin intalerance. These data demanstrate
that the nasal palyps as well as aspirin intalerance faund
in asthmatic patients usually indicates the presence af
a severe asthmatic state.
The frequency af nasal palyposis in children is ex-
TABLE I
Frequency of Nasal Polyps in Various Conditions
N
asal palyps are frequently bilateral and multiple
and have a characteristic appearance. They are
glistening, pale gray, smaath, saft, semitranslucent,
freely mavable, attached by a pedicle, and arise fram
the surfaces af the middle turbinates, the hiatal semi-
lunaries, ar astia afthe ethmaid and maxillary sinuses.
They are mast cam manly faund in the middle meatus
extending to.the nasal cavity filling the nase, and finally
pratruding fram the anteriar nares. If the palyp prajects
pasteriarly into. the nasapharynx, it is called a chaanal
palyp, which may nat be seen by rautine examinatian
through the anteriar nares. Chaanal palyps may be
single, usually accur during the first twa decades af life,
TABLE III
Frequency of Nasal Polyps in Various Age Groups of
Asthmatic Patients
Age When No. with
First Seen No. with Nasal
(yr) Asthma Polyps % p

Diagnosis
Frequency
(%)
10-19
20-29
30-39
491 )
465
418
1,374 ,:)
16
43
1.8 )
3.9
3.8
3.]
<0.01*
I. Aspirin intalerance 36 40-49 410 } 41 } 10.0 }
2. Adult asthma 7 50 and 444 854 65 106 14.6 12.4
a. Intrinsic asthma 13 over
b. Ato.pic asthma 5 Total 2,228 149 6.7
3. Chronic rhinitis 2 * The difference between the 1O-39-year-old group (43/1,374). 3.1%,
a. Nanallergic rhinitis 5 compared to the 40-year-old and over group (106/854), 12.4%, is
b. Allergic rhinitis 1.5 statistically significant.
4. Childhaad asthma/rhinitis 0.1 Reprinted from Settipane GA, Chafee FH. Nasal polyps in asthma
and rhinitis: a review of 6,037 patients. J Allergy Clin Immunol
5. Cystic fibrosis 20
59:17-21, 1977

TABLE II

Frequency of Nasal Polyps in Asthma and Rhinitis

Positive Allergy Skin Negative Allergy Skin Total

Total Tests Tests _ Polyps_
Diagnosis Patients No. Polyps % No. Polyps % p No. % p
Asthma 2,228 1,717 85 5.0 511 64 12.5 <0.01 149 6.7
Rhinitis anly 2,758 2,126 32 1.5 632 30 4.7 <0.01 62 2.2 <0.01*
Total 4,986 3,843 117 3.01,143 94 8.2 2114.2
* The difference in the frequency of nasal polyps in asthma (6.7%) compared to rhinitis (2.2%) is statistically significant.
(Reprinted with permission from Settipane GA, Chafee FH. Nasal polyps in asthma and rhinitis: a review of 6,03 7
patients. J Allergy Clin ImmunoI59:17-21, 1977.)

120 Fall 1987, Vel. 1, No.. 3

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and are classified in three groups: I) antrochoanal pol-
yps arising from the antrum; 2) polyps arising from
other sinuses; or 3) polyps, which are the posterior part
of multiple ethmoidal polyps. Polyps are one of the
most common types of mass found in the nasal passage.
HISTOPATHOLOGY
H istorically, nasal polyps have pseudostratified co-
lumnar epithelium and cellular constituents of
normal nasal mucosa. Polyps from patients who do not
have cystic fibrosis have extensive thickening of the
epithelial basement membranes with extension into the
submucosa as an irregular hyaline membrane, high
stromal eosinophil count, and mainly neutral mucin in
mucous glands, cysts, and mucous blanket.8 Glands are
few and denervated. Polyp tissue is essentially free of
nerve endings, except for nerve terminals in the base of
the polyp associated with blood vessels. In most cases,
the cells consist of a mixture of lymphocytes, plasma
cells, and eosinophils. Occasionally, neutrophils are
numerous. Nasal smears from these patients usually
reveal "sheets" of eosinophils. In contrast, polyps from
patients with cystic fibrosis have a delicate, barely visi-
ble basement membrane of surface epithelium without
submucosal hyalinization, lack of extensive infiltration
of eosinophils, and a preponderance of acid mucin in
glands, cysts, and surface mucosa blanket. Polyps from
patients with Kartagener's and Young's syndromes usu-
ally lack an eosinophilic component and have neutro-
phils as the predominant cell.
In non-cystic fibrosis polyps, one report9 demon-
strated that all polyps showed evidence of epithelial
damage, either ulceration or marked desquamatization.
In another study, 10 a small proportion of polyps showed
a focal dysplastic change of the surface lining of the
mucosa with no related changes in the immediately
underlying stroma. On follow-up, in none of these
patients did an invasive feature supersede, and these
changes appear to constitute a local reaction to recur-
rent irritation.
DIFFERENTIAL DIAGNOSIS
T he differential diagnosis of nasal polyps includes
chordoma, chemodectoma, neurofibroma, angiofi-
broma, inverting papilloma, squamous cell carcinoma,
sarcoma, and encephaloceles or meningoceles. Most of
these lesions present as unilateral lesions. Meningoceles
enter the nasal cavity via the cribriform plate. They
increase in size with straining, lifting, or crying and
may have a pulsating characteristic. The other lesions
included in this differential diagnosis are not mobile,
bleed easily, and may be sensitive to manipulation.
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Nasal polyps are characteristically mobile, rarely bleed,
are not sensitive to manipulation, and are frequently
bilateral and multiple. Malignant tumors frequently are
associated with bony, destructive changes. In rare cases,
benign paranasal sinus cysts or polyps may also produce
bone destruction (Woakes disease).11 Diagnostic pro-
cedures include angiography, tomographic x-rays, com-
puterized tomography scan, and biopsy.
ASSOCIATION WITH SYSTEMIC DISEASES
T he most common systemic disease associated with
nasal polyps is nonallergic asthma, followed by
aspirin intolerance. The triad of nasal polyps, asthma,
and aspirin intolerance will be discussed in a separate
category later on in this review. Patients with cystic
fibrosis have a high frequency of nasal polyps (20%).
Children age 16 or younger who have nasal polyps
should be evaluated for cystic fibrosis. Similar to cystic
fibrosis, the polyps associated with the chronic dyski-
netic cilia syndrome and Young's syndrome have the
neutrophil as the predominant cell.
Primary ciliary dyskinesia is classically manifested in
Kartagener's syndrome, which is an uncommon genetic
condition with an estimated incidence of 1 in 20,000
births.Il,12 It appears to be inherited as an autosomal
recessive trait and is characterized by bronchiectasis,
chronic sinusitis, and situs inversus (complete reversal
of internal organs with heart on the right, liver on the
left, etc.). The ciliary abnormality in these cases usually
involves the entire body including the respiratory tract
and sperm cells. The disorder is in the cilia itself in
which the dynein arms are missing and the celia re-
mains completely immotile. Situs inversus is found in
only 50% of patients with this syndrome. Infections
caused by Pseudomonas aeruginosa is often found in
patients with Kartagener's syndrome or cystic fibrosis. 13
Young's syndrome consists of recurrent respiratory
diseases, azoospermia, and nasal polyposis. The respi-
ratory disease consists of severe chronic sinusitis which
may be associated with bronchiectasis!4,lS These pa-
tients have normal sweat chloride values and pancreatic
function and, therefore, do not have a variant of cystic
fibrosis. Cilia structures are normal in sperm tails taken
from testicular biopsy specimens and in cilia from
tracheal biopsy specimens and, therefore, these patients
do not have a chronic form ofimmotile cilia syndrome.
The azoospermia is due to a block in the epididymis
that is distinguishable from the defect in the vas defer-
ens associated with cystic fibrosis. However, spermato-
genesis is normal. The prevalence of Young's syndrome
is considerably higher than that of cystic fibrosis or
Kartagener's syndrome. It is responsible for 7.4% of
cases of male infertility. '
Thus, it is apparent that the presence of nasal polyps
121
may be a sign that a basic generalized disease may be
present and that the nasal polyp may represent just the
tip of a deep iceberg. The systemic diseases that are
associated with nasal polyps are listed in Table IV and
are in the order of frequency found in the general
population.
CHEMICAL MEDIATORS
C hemical mediators found in nasal polyps are hista-
mine, serotonin, leukotrienes [(slow reactive sub-
stance of anaphylaxis, LTC, LTD4, LTE4), LTB4],
eosinophilic chemotactic factor of anaphylaxis (ECF-
A), norepinephrine, kinins, TAME-esterase, and possi-
bly prostaglandin PGD2.
Kaliner et al.18 reported that the release of chemical
mediators in nasal polyps is modulated by agents af-
fecting the intracellular concentrations of cyclic nucleo-
tides. These authors also stated that the quantity of
SRS-A released in relation to the amount of histamine
released from nasal polyps is considerably less than that
released from the human lung. Bumsted et al. 17reported
that there is more histamine in nasal polyps than in
normal mucosa and that norepinephrine is present in
greater concentration in the base of nasal polyps than
in normal mucosa. However, there is no difference in
serotonin levels in nasal polyps and normal mucosa. In
addition, there is no difference in levels of histamine,
serotonin, and norepinephrine in nasal polyps from
groups of patients with or without inhalant allergies or
asthma. An interesting finding is that patients with
aspirin intolerance have levels of histamine in nasal
polyps that are much lower than all other types of
patients with nasal polyps, approximating the histamine
levels found in normal mucosa. Chandra and Abrol19
reported that polyp fluid contains albumin and immu-
noglobulins (IgA, IgE, IgG, IgM, and macroglobulins).
The concentrations of 19A and IgE and, in some
TABLE IV
Nasal Polyps Associated with Systemic Diseases*
I. Asthma (nonallergic)
2. Aspirin intolerance (bronchospastic type)
3. Samter's triad (asthma, aspirin intolerance, and na-
sal polyps)
4. Young's syndrome (sinopulmonary disease, azoo-
spermia, nasal polyps)
5. Cystic fibrosis
6. Kartagener's syndrome (bronchiectasis, chronic si-
nusitis, and situs inversus)
* The first three diseases are associated with tissue
eosinophilia while in the latter group oj diseases the
predominant cell is the neutrophil.
122
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cases, IgG and IgM were greater in the polyp fluid than
in the serum. Using the Prausnitz-Kustner procedure,
Berdal20 in 1952 reported that skin sensitivity antibody
in polyp fluid was many times more concentrated than
that found in sera. An explanation for these increased
concentrations of serum components found in polyp
fluid may be that the polyp may act as a dialyzing
membrane with water evaporating through the mucosa.
PATHOGENESIS
A current theory on the pathogenesis of polyps has
been presented by Bumsted et a1.17Their theory is
based on data that norepinephrine is present in greater
concentration in the base of nasal polyps than in normal
mucosa. They stated that this norepinephrine at the
base of the polyp could produce excessive a-adrenergic
receptor-mediated vasoconstriction that might lead to
rebound mucosal congestion and edema, and this po-
tentiates the effects of histamine and kinins. Norepi-
nephrine through a-adrenergic receptor activation
would lower the effects of cyclic adenosine monophos-
phate, which would enhance the release of histamine,
SRS-A, and ECF-A. These mediators would cause an
increased vascular permeability, edema, and the leakage
of macromolecules out of the vascular system eventu-
ally causing the polyp formation. They explain the
lower levels of histamine found in polyps of aspirin-
intolerant patients, by stating that these patients have
an increased sensitivity to histamines.
Mygind21 feels that polyp formation is related to
denervation of blood vessels and degranulation of mast
cells in the nasal mucosa. This process leads to increased
vascular permeability, edema, and finally polyp for-
mation. He lists causative factors for denervation to be
infection, cystic fibrosis, and aspirin intolerance. He
lists contributing factors for mast cell degeneration as
IgE-dependent reactions.
An old theory22 on polyp formation deals with Ber-
noulli's theorem which states that gases or fluid passing
through a constrictor results in an area of negative
pressure in its vicinity. Weakened, denervated tissue
such as polyps may theoretically be sucked out by this
negative pressure leading to edema and enlargement of
the polyp.
None of these theories appears adequate to account
for all of the known facts involving nasal polyps. How-
ever, the theory of Bumsted et al.17 is more closely
related to biochemical events and perhaps with some
modification may be more plausible. The fact that nasal
polyps are frequently associated with systemic diseases
indicates that the underlying cause of polyposis may be
related to a basic generalized biochemical disorder. At
the present time, the pathogenesis of polyp formation
is unknown.
Fall 1987, Vol. 1, NO.3
RELATIONSHIP OF ATOPY
TABLE VI
N asal polyps are more frequently found in asth-
matic/rhinitis patients who have negative skin
tests rather than those with positive skin tests (Table 167 Patients with Verified Polyps and
II). There is a relationship to asthma in that over 70% Polypectomies3!
of patients with nasal polyps have an associated asthma
Total No. of No. of
(Table V). Some patients with nasal polyps not only
Patients Polypectomies Patients %
have no history of asthma but also have negative meth-
acholine challenge tests.23.24Therefore, not all patients 167 lor more 143 86
with nasal polyps have an associated lower respiratory 143 2 or more 57 40
disease.25 Whiteside et al.26 reported that in five of six 143 3 or more 34 24
cases of nasal polyps in nonatopic patients, no IgE- 143 4 or more 22 15
bearing lymphocytes were detected in the polyp tissue. 143 5 or more 17 12
However, in atopic patients, 19E-bearing lymphocytes 143 6 or more 11 8
in nasal polyps correlated well with serum 19E levels.
We reviewed27 167 patients with nasal polyps and
143 (86%) of these had one or more polypectomies reflects the positive allergy test frequency in the larger
(Table VI). A number of these patients had a verified population from which these polyp cases were obtained
history of two, three, four, or even five or more poly- and is not directly related to polyp formation.
pectomies. Our preliminary data suggest that patients It appears that atopy or IgE-mediated disease is not
with positive allergy skin tests (pollen, animal dander, a cause of nasal polyps, but once polyp formation
or molds) have a progressively higher rate of repeated occurs, atopy or 19E-mediated disease may aggravate
polypectomies (Table VII). However, this trend is not and increase the risk of nasal polyp formation. Acute
statistically significant possibly because of the small upper respiratory infections, are also known to cause
number of patients involved in some categories. an exacerbation or enlargement of nasal polyps.27
The frequency of one or more positive allergy skin
tests (pollens, danders, or molds) in our patient popu- RELATIONSHIP TO ASPIRIN INTOLERANCE
lation with nasal polyps is 56%.2 However, this popu-
lation was obtained from allergy patients, both in pri- T he full blown triad of asthma, aspirin intolerance,
and nasal polyps usually is associated with a severe
vate practice and in the allergy clinic at Rhode Island type of asthma that is frequently steroid-dependent.
Hospital where the overall frequency of one or more This type of asthma has the bronchospastic type of
positive allergy skin tests was 77%.2 Therefore, the 56% aspirin intolerance, not the urticaria/angioedema type
positive allergy skin tests in patients with nasal polyps (Table VIII). In many cases, only two legs of the triad
are present-asthma and aspirin intolerance-which
usually occur within I year of each other. Nasal polyps
may occur about 10 years later (Table IX).28The mean
TABLE V age of onset of the asthma and aspirin intolerance part
ofthe triad is about 31 years.29 However, the cumulative
Nasal Polyps (211 Cases): Characteristics frequency increases with age so that in patients older
than 40, the frequency is 10% and above.
Clinical Categories No. %
Other characteristics of this triad are listed in Table
Males 106 50.2 IX. It is most commonly associated with nonallergic or
Females 105 49.8 negative skin test asthma and with a normal serum 19E
Asthma 149 70.6 level. Specific IgE against aspirin has not been found.
Rhinitis (alone) 62 29.4 During acute bronchospasm produced by aspirin chal-
Positive allergy skin tests 117 55.5 lenge, histamine levels, neutrophil chemotactic activity,
Total aspirin intolerance 30 14.2 and complement activation were not found to be sig-
Subtypes of aspirin intolerance nificantly different from baseline levels.30 Elevated
Bronchospasm 21 70.0 blood eosinophils and a marked eosinophilia in the
Urticaria 4 13.3 nasal secretions are also characteristic of this syndrome.
Both bronchospasm and urticaria 2 6.7 There is a hereditary disposition of aspirin intolerance
Rhinitis 3 10.0 in that clusters of this syndrome are found in certain
families.29 The frequency of aspirin intolerance in-
Reprintedfrom Settipane GA, Chafee FH. Nasal polyps
creases with age, especially over 40. Also, it is the
in asthma and rhinitis: a review oj 6,037 patients. J
bronchospastic type of aspirin intolerance not the urti-
Allergy Clin ImmunoI59:17-21, 1977.
caria/angioedema type that increases with age.

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 TABLE VII TABLE VIII

Frequency of Polypectomies in Patients with Positive Characteristics of the Bronchospastic Type of Aspirin
Allergy Skin Tests Intolerance

No. with Found in asthmatic patients

No. of Total Positive Allergy Correlated with nasal polyposis
Polypectomies Patients· Skin Tests % Similar age onset as asthma
Severe rhinorrhea with aspirin reactions
None 24 12 50
Increased frequency in older age groups
One or more 143t 81 57
Familial occurrence
Two or more 57 33 58
Eosinophil in nasal smear
Three or more 34 20 59
Elevated total (blood) eosinophil count
Four or more 22 15 68 Nonsteroidal anti-inflammatory drug cross-reaction
Five or more 17 12 71
No specific IgE (anti-aspiryl)
Six or more 11 8 73
Normal total IgE
* Total patients = 167. Desensitization possible to aspirin
t One patient did not have a skin test (81/142 = 57%). Pathogenic mechanism: prostaglandins

Contrary to previous opinion, the surgical removal
of nasal polyps does not cause or aggravate asthma
(Table X). In our laboratory, 10 patients with nasal
polyps and no history of asthma were studied. Results
of methacholine challenge tests done before and about
5 months after polypectomy were similar.23 In a report
by Miles-Lawrence et a1.,24similar data were obtained.
They performed methacholine challenge tests 1 month
prior to polypectomy and up to 1 year following pol-
ypectomy. They found essentially no change in meth-
acholine sensitivity, confirming our conclusion that
polypectomy does not cause or worsen asthma. How-
ever, the occurrence rate for nasal polyps following
polypectomy is notoriously high and may be aggravated
by many nonspecific factors such as upper respiratory
infection and allergies to pollens, danders, and molds
(when the chance occurrence of these diseases coex-
istS).27.31
To extend these laboratory findings to clinically rel-
evant data, we evaluated pulmonary function tests just
prior to polypectomy and up to 5 months following
polypectomy. There was no significant change in pul-
monary function tests.28
We also evaluated seven steroid-dependent asthmatic
patients for steroid requirements before and approxi-
mately 1 month following polypectomy (Table XI).
The steroid requirements were essentially unchanged
in five patients and decreased in two, possibly because
of less stimulation through the rhinosinobronchial re-
flex. Thus, our initial data with methacholine sensitivity
has been confirmed with subsequent clinical informa-
tion.
It is important to remember that nonsteroidal anti-
inflammatory drugs (NSAID) cross-react with aspirin
and cause a similar acute bronchospasm in aspirin-
intolerant asthmatics. These drugs are cyclooxygenase
inhibitors. Some of these NSAID, such as indomethacin
and ibuprofen, cross-react with aspirin in intolerant
individuals about 100% of the time. Other NSAID
cross-react with aspirin in intolerant individuals at a
somewhat decreased rate.
The pathological mechanism of aspirin intolerance is
unknown. A recent pathogenic hypothesis for aspirin
intolerance is based on the association between prosta-
glandin and SRS-A. It is possible that in certain indi-
viduals, inhibition of the cyclooxygenase pathway may
cause a preference for the lipoxygenase resulting in
increased production of leukotrienes LTC4, LTD4, and
LTE4 (SRS-A), which will produce bronchospasm. An-
other mechanism implies that a decrease in PGE allows
the bronchospastic effects of PGF and leukotrienes to
predominate. A similar mechanism including arachi-
donic acid and prostaglandins for the formation of nasal
polyps has not been developed at this time, but further
research is needed in this area.
TREATMENT
P olypectomy is not the treatment of choice for rou-
tine nasal polyposis. We reviewed 167 patients with
verified nasal polyps (Table VI). Eighty-six percent
(143) had polypectomies. Of these 143, 57 (40%) re-
quired two or more polypectomies, 34 (24%) required
three or more polypectomies, 22 (15%) required four
or more polypectomies, 17 (12 %) had five or more
polypectomies, and 11 (8%) had six or more polypec-
tomies. Three of our patients had a history of 20 or
more polypectomies. Therefore, nasal polyposis fre-
quently is a recurrent problem in over 40% of the cases.
Other studies19 have found a recurrence rate of over
31 %. Surgical polypectomy does not permanently elim-

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inate this disease. However, in certain selected cases,
especially in those in whom corticosteroids are not
effective or are contraindicated, surgical polypectomy
may be considered. Steroid injection or nasal polyps
has been used with some success in the hands of expert
otolaryngologists.32 However, injection of steroids in
the nasal turbinates and polyps has resulted in 10
instances of visual loss, five of which were permanent
as of 1981.33 Steroid emboli were demonstrated in the
retinal vessels in six cases. Certainly, this type of treat-
ment for nasal polyps should be reserved for the very
skilled otolaryngologist if it is used at all.
At the present time, I feel that the treatment of choice
is a 10-day course of systemic corticosteroid therapy
beginning with about 50 mg of prednisone orally and
decreasing by 5 mg daily. This short burst of corticoste-
roids should not cause a clinically significant suppres-
sion of the pituitary-adrenal axis. Afterwards, patients
may be maintained on topical beclomethasone or flu-
nisolide, realizing that long-term use of these topical
medications may result in suppression of the pituitary-
adrenal axis. Newer products such as topical fluocortin
butyl may help to solve these complications since this
steroid has not been found to have a sig-
nificant pituitary-adrenal effect. Fluocortin butyl is still
undergoing clinical investigation and has not been re-
leased to the practicing physician in the United States
yet.
Even with systemic and topical corticosteroid ther-
apy, nasal polyps frequently may still be a recurrent
disease and periodic bursts of systemic corticosteroids
may have to be administered. When treatment with
systemic corticosteroids has no effect, or is contraindi-
cated, a surgical procedure may be contemplated.
Patients with nasal polyps deserve an allergic evalu-
ation despite the fact that a large percentage of them
are nonatopic. If clinically relevant IgE-mediated dis-
ease is found in these patients, a course of hyposensiti-
zation may be given, especially in those with recurrent
polyposis. IgE-mediated disease is not the cause of nasal
polyps, but it may contribute to episodes or exacerba-
tion.25

TABLE XI
TABLE IX
Effect of Polypectomy on Steroid-Dependent Asthma
Asthma with Nasal Polyps: Onset of Polyps versus (6-month interval)
Onset of Asthma
Prednisone
Mean Age Postoperative Change in
Time Patient (yr) Preoperative (6 mol Asthma
Interval Range
M.S. 48 10 mg alt days 10 mg alt days Same
between of Time
P.B. 25 10 mg alt days 10 mg alt days· Same
Initial Total Diagnosis Interval L.c. 66 10 mg alt days 2.5 mg daily Better
Diagnosis Patients % (yr) (yr) P.M. 66 5 mg daily 10 mg alt days Better
Polyps (first) 35 29.4 11.2 1-46 F.S. 42 10 mg alt days 10 mg alt days Same
Asthma (first) 73 61.3 9.5 1-37 V.L. 58 10 mg daily 10 mg daily Same
Both together 11 9.2 0 J.e. 76 10 mg alt days 10 mg alt days Same
Total 119 • Data collected at 9 months.

TABLE X

Effect of Polypectomy on Methacholine Sensitivity

Methacholine Sensitivity Time

Investigators
Downing, Braman, Settipane
(1982)23
Miles-Lawrence, Kaplan,
Change (1982)24
* Two patients followed for
Interval
Total after
Patients Diagnosis Same Increased Decreased Polypectomy
6 No asthma 6 0 0 Mean 20 wk
4 Asthma 2 1 1 Mean 20 wk
5 No asthma 2 1 2 1 mo·
1 Asthma 0 1 0
6 and 12 months, respectively, had no change in methacholine sensitivity.

American Journal of Rhinology 125

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SUMMARY
N asal polyps frequently are associated with aspirin
intolerance, intrinsic asthma, Young's syndrome,
cystic fibrosis, and Kartagener's syndrome. Children 16
years or younger with nasal polyps should be evaluated
for cystic fibrosis. Nasal polyps are frequently bilateral,
multiple, freely movable, and pale-gray and arise from
the middle meatus of the nose. Histologically, they
classically have pseudostratified ciliated columnar epi-
thelium, thickening of the epithelial basement mem-
brane, high stromal eosinophil count, mucin with neu-
tral pH, few glands, and essentially no nerve endings.
Cells consist of a mixture of lymphocytes, plasma cells,
and eosinophils. Polyps from patients with Young's
syndrome, Kartagener's syndrome, and cystic fibrosis
have predominately neutrophils with insignificant eo-
sinophils. Chemical mediators found in nasal polyps
are as follows: histamine, serotonin, leukotrienes [(SRS-
A or LTC4, LTD4, LTE4), LTB4], ECF-A, norepineph-
rine, kinins, TAME-esterase, and possibly PGD2• There
is more histamine in nasal polyps than in normal nasal
mucosa, and norepinephrine is present in greater con-
centration in the base of nasal polyps than in normal
mucosa. The concentrations of IgA and IgE and, in
some cases, IgG and IgM are greater in polyp fluid than
in serum. IgE-mediated disease is not the cause of nasal
polyps, but when present, may contribute to episodes
of exacerbation. Despite medical or surgical manage-
ment, a significant number of nasal polyps are recur-
rent. For treatment, systemic corticosteroids should be
tried before surgical polypectomy. Polypectomy does
not increase the risk of developing asthma or making
asthma worse. At the present time, the pathogenesis of
polyp formation is unknown.
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